I Accid Emerg Med 1999;16:433-439

ECG INTERPRETATION FOR THE EMERGENCY DEPARTMENT

Electrocardiographic ST segment elevation inadults with chest pain

William J Brady, Francis Morris

The accident and emergency (A&E) physicianmust be an expert in the interpretation of theelectrocardiogram (ECG). Patients with chestpain and ST segment elevation on the 12 leadECG who are experiencing acute myocardialinfarction (AMI) may be candidates for urgentcoronary revascularisation via either throm-bolysis or primary angioplasty. Such treatment,to maximise benefit, must be delivered as earlyas possible after the onset of infarction. Othersuch patients with chest pain and electrocar-diographic ST segment elevation may besuffering from a non-coronary chest discom-fort syndrome. The correct identification ofthese patients-both clinically and electro-cardiographically-must be made in order tooffer the most appropriate treatments and toavoid potentially dangerous therapies. TheA&E doctor is frequently the initial clinicianwho examines the chest pain patient, interpretsthe ECG, and makes these early therapeuticdecisions. Accurate interpretation of the ECGand the correct diagnosis of AMI among thenumerous causes of ST segment elevation is amandatory skill. The ability of the doctor tocorrectly interpret the electrocardiographicfindings in such patients directly and immedi-ately impacts on management decisions as wellas influences patient outcome."A The followingdiscussion focuses on the differential diagnosis

Departmnent ofEmergency Medicine,University ofVirginiaSchool ofMedicine,Charlottesville,Virginia, USAW J Brady

Department ofAccident andEmergency Medicine,Northern GeneralHospital, SheffieldF Morris

Correspondence to:Dr William J Brady,Department of EmergencyMedicine, Box 523-21,University of Virginia HealthSciences Center,Charlottesville, VA 22908,USA (e-mail:wb4z@,hscmail.mcc.virgina.edu).

Accepted 21 August 1999

of ST segment elevation in the patient withchest pain.

Case reportsCASE 1A 38 year old African man presented to theA&E department with central chest pain. Thepain had started at rest and was associated withsweating. No past history nor family history ofischaemic heart disease was noted. Examina-tion revealed a harsh systolic murmur at theleft sternal edge. The ECG (fig 1) was initiallyinterpreted as demonstrating ST segmentelevation in leads V1-V3, compatible withAMI. The patient was prescribed thrombolysis(streptokinase 1.5 megaunits) and referred tothe coronary care unit. Subsequent evaluationrevealed that he had a significant aortic steno-sis. No evidence of AMI was found. RepeatECGs did not reveal any evolving changes andcardiac enzymes were never raised. He had nofurther chest pain. The initial ECG wasreinterpreted as demonstrating evidence of leftventricular hypertrophy. The ST segmentelevation in leads V1-V3 was thought to beentirely compatible with this diagnosis and notsuggestive of an AMI.

Figure 1 Left ventricular hypertrophy: normal sinus rhythm with the cardinalfeatures ofleft ventricular hypertrophy. TheST segment elevation apparent in leads V1-V2 is compatible with the repolarisation changes of left ventricularhypertrophy.

433

I

on Septem

ber 18, 2020 by guest. Protected by copyright.

http://emj.bm

j.com/

J Accid E

merg M

ed: first published as 10.1136/emj.16.6.433 on 1 N

ovember 1999. D

ownloaded from

Brady, Morris

I aVR Vi V4

11 aVL V2 V5

III aVF V3 V6

IJ

Figure 2 Benign early repolarisation (BER): normal sinus rhythm with ST segment elevation in leads V2 -V4. The STsegment elevation is concave upwards and, in lead V3, a notch is evident at the point. The ECG changes did not evolveover time. The final electrocardiographic diagnosis is BER.

CASE 2A 48 year old man presented in the early hoursof the morning with retrosternal burningdiscomfort. The pain had started six hourspreviously after a large meal and was unre-lieved by antacids. The pain had prevented himfrom sleeping and he was particularly uncom-fortable in bed. There was no significant pastmedical history apart from an acute attack ofgout three months previously. Clinical exam-ination was normal. The ECG (fig 2) wasthought to demonstrate ST segment elevationcompatible with an anterior AMI and he wasreferred to coronary care for thrombolysis. Onfurther evaluation, it was thought that the STsegment elevation was a manifestation ofbenign early repolorisation (BER) rather thanAMI. Serial ECGs did not reveal any evolutionof the ST segment elevation and there was nocardiac enzyme rise. A stress test seven daysafter admission did not reveal any significantischaemia.

CASE 3A 64 year old woman presented to the A&Edepartment with substernal chest pain, similarto previous attacks of angina. The pain wasassociated with nausea and sweating. She had apast history of AMI, diabetes, and hyper-tension. A 12 lead ECG showed sinus rhythmwith ST segment elevation in leads III and aVFconsistent with AMI (fig 3). The patient wasreferred to the coronary care unit for throm-bolysis, which was applied without complica-tion or apparent change in the patient's condi-tion. Further study of her medical historyrevealed past inferior wall AMI with aneurysm.Serial ECGs did not demonstrate change andcardiac enzymes did not rise; an echocardio-gram revealed inferior dyskinesis consistentwith inferior wall aneurysm.

CASE 4A 43 year old female without a past medicalhistory presented with left chest pain. The pain

Figure 3 Left ventricular aneurysm: normal sinus rhythm with ST segment elevation in leads III and aVFI Comparisonwith serial ECGs as well as a previous ECG did not demonstrate any change. Review ofpast medical records revealed ahistory of inferior wallAMI with aneursym.

434

on Septem

ber 18, 2020 by guest. Protected by copyright.

http://emj.bm

j.com/

J Accid E

merg M

ed: first published as 10.1136/emj.16.6.433 on 1 N

ovember 1999. D

ownloaded from

ST segment elevation syndromes

Figure 4 Acute pericarditis: widespread ST segment elevation is seen in leads V2 to V6 as well as the inferior leads. Theinitial up-sloping portion of the ST segment is concave, suggesting a non-infarction cause of the electrocardiographicabnormality. Additionally, PR segment depression is seen in leads II, III, and aVF Reciprocal changes are noted in leada VR: PR segment elevation and ST segment depression.

had appeared approximately two to three daysbefore arrival; the pain was worsened uponinspiration, assuming the supine position, andwith upper extremity movement; no otherassociated symptoms were noted. The patienthad recently experienced an upper respiratoryinfection. The physical examination was nor-mal; no chest wall tenderness was found. AnECG (fig 4) revealed normal sinus rhythm withwidespread ST segment elevation. The pa-tient's pain lessened considerably on treatmentwith a non-steroidal anti-inflammatory agentand morphine sulphate. The patient wasadmitted to the cardiology service for 24 hourobservation and discharged without incident.

Table 1 Clinicalsyndromes in the chest painpatient which may casueSTsegment elevation

Acute myocardial infarctionVariant anginaAcute pericarditisBenign early repolarisationLeft ventricular hypertrophyBundle branch blockCardiomyopathyAcute myocarditisLeft ventricular aneurysmPre-excitation syndromesHyperkalaemiaHypothermiaCentral nervous system

DiscussionIn the evaluation of patients with chest pain,the A&E doctor uses three principle tools: thehistory of the event, the 12 lead ECG, andserum markers of myocardial injury. The clini-cal history is the most vital assessment tool, yetthe ECG is an important adjunct and mayinfluence clinical management. ST segmentelevation is perhaps the "most demanding" ofthe electrocardiographic features seen in thechest pain patient; it is "demanding" in that itspresence must be explained and, if theaetiology involves AMI, urgent therapeuticdecisions must be made.

.l

+AMI Pericarditis

Unfortunately, ST segment elevation is a notuncommon finding on the ECG of the patientwith chest; its cause infrequently involves AMI.In fact, such patients may present electrocar-diographically with ST segment elevationbecause of either AMI, confounding patterns,and/or masquerading syndromes. In mostinstances, ST segment elevation resulting fromAMI is easily noted. Confounding patternssuch as left bundle branch block, ventricularpaced rhythms, and left ventricular hypertro-phy may obscure the typical electrocardio-graphic findings of AMI as well as producenon-infarctional ST segment elevation whichmay lead the uninformed doctor astray. OtherST segment elevation patterns, including beBER and acute pericarditis, occur in theindividual with chest discomfort and may sug-gest the incorrect diagnosis of AMI. Refer tofig 5 for a depiction of ST segment elevationtypes for various clinical syndromes and tables1 and 2 for a listing of these syndromes.The occurrence of numerous other non-

infarctional ST segment elevation syndromesonly reinforces the point that ST segmentelevation is an insensitive marker ofAMI.s Onepre-hospital study of adult chest pain patientsin North America demonstrated that themajority of patients manifesting ST segmentelevation on the ECG did not have AMI as a

4A

BER BBB LVH V pacedevents

Acute abdominal disorder Figure 5 Electrocardiographic syndromes presenting with ST segment elevation (AMI = acute myocardial infarction;BER = benign early repolarisation;BBB = bundle branch block; LVH = left ventricular hypertrophy).

435

on Septem

ber 18, 2020 by guest. Protected by copyright.

http://emj.bm

j.com/

J Accid E

merg M

ed: first published as 10.1136/emj.16.6.433 on 1 N

ovember 1999. D

ownloaded from

Brady, Morris

Table 2 Causes ofST segment elevation among patientswith chest pain in the emergency department: 902 patientspresented with chest pain; 202 (22%) patients showed STsegment elevation on the ECG; the responsible aetiologiesare listed below'

Syndrome Patients (0o)

Left ventricular hypertrophy 25Left bundle branch block 15Acute myocardial infarction 15Benign early repolarisation 12Right bundle branch block 5Intraventricular conduction delay 5Aneurysm 3Pericarditis 2Undefined 1 8

~LLLaVR VI V4

2fW~~~~~~V

Figure 6 ECG demonstrating left ventricular hypertrophy related repolarisation chparticularly ST segment elevation in leads Vl-V3 with ST segment depression in tilateral distribution. Prominent ST segment elevation is seen in the right to mid-precleads; the initial up-sloping portion of the ST segment is concave, which suggests anon-infarction cause of the ST segment change.

B.

_TI

C

Figure 7 (A) and (B) Right precordial leads with pronounced ST segment elevat,

concave ST segment morphology. (C) The concept of appropriate discordance in thi

with left ventricular hypertrophy who has had an ECG states that the terminal por,

the QRS complex (arrowed B) and ST segmentIT wave (arrowed A) are located o:

opposites sides of the isoelectric baseline. In the right to mid-precordial leads, QS co?

(predominantly negative QRS complexes), pronounced ST segment elevation is enc,

as predicted by the concept of appropriate discordance. The initial, up-sloping portic

ST segmentIT wave is concave (small arrows), which suggests a non-infarction cau~

ST segment elevation.

zanges,

final hospital diagnosis; rather, left ventricularhypertrophy and left bundle branch blockaccounted for the majority of the cases.6Further, in a North American review of adultpatients presenting to the emergency depart-ment with chest pain and ST segmentelevation on the ECG, ST segment elevationresulted from AMI in only 15% of this popula-tion; left ventricular hypertrophy, seen in 30%of adult chest pain patients, was the mostfrequent cause of this ST segment elevation (WJ Brady. Abstract presented at InternationalEmergency Medicine Conference, Vancouver,Canada, 26 March 1998). In the coronary careunit population, Miller et al demonstrated thatST segment elevation was diagnostic for acuteinfarct in only half of patients with a pasthistory of ischaemic heart disease with such STsegment changes.7 These syndromes causingST segment elevation not related to AMI arenot infrequently misdiagnosed as acute infarc-tion, which then may subject the patient tounnecessary and potentially dangerous treat-ments and procedures. For example, a reportby Sharkey et al noted that 11% of patientsreceiving thrombolytic agent were not experi-encing AMI. The electrocardiographic syn-dromes producing this pseudoinfarct ST seg-ment elevation included BER (30%), leftventricular hypertrophy (30%), and variousintraventricular conduction abnormalities(30%).8

be LEFT VENTRICULAR HYPERTROPHYordial Electrocardiographic changes related to left

ventricular hypertrophy are uncommonly en-countered in the A&E chest pain patient. STsegment elevation is seen frequently in patients

v,\ with pre-hospital chest pain and, in fact, is the\et leading cause of such non-infarctional ST seg-

ment change.6 Among patients with chestA discomfort, left ventricular hypertrophy is

responsible for approximately 25% of non-infarctional ST segment elevation (W J Brady.

\ Abstract presented at International EmergencyB Medicine Conference, Vancouver, Canada, 26B March 1998). Its presence on the ECG,

particularly the repolarisation changes thatalter the morphology of the ST segment and/orthe T wave, may confound the early evaluation

\ of the chest pain patient. Larsen et al haveshown that the electrocardiographic pattern

A consistent with left ventricular hypertrophy isencountered in approximately 10% of adultchest pain patients initially diagnosed with

\ acute ischaemic heart disease.9 After hospitaladmission and more extensive evaluation, only

B one quarter of these patients were found tohave AMI. The remainder of the patients-thevast majority-were ultimately diagnosed withnon-ischaemic syndromes. The physicians car-ing for the patients in this study incorrectlyinterpreted the ECGs more than 70% of the

*ion and time. They frequently did not identify the lefte patient ventricular hypertrophy pattern and thereforetion of attributed the ST segment/T wave changes tomplexes ischaemia or infarction-when in fact theountered observed ST segment/T wave changes resultedse of the from repolarisation abnormality associated

with left ventricular hypertrophy.9

A

A

436

L

on Septem

ber 18, 2020 by guest. Protected by copyright.

http://emj.bm

j.com/

J Accid E

merg M

ed: first published as 10.1136/emj.16.6.433 on 1 N

ovember 1999. D

ownloaded from

ST segment elevation syndromes 437

Figure 8 Various electrocardiographic complexesdemonstrating BER. In each case, ST segment elevation isseen with prominent Jpoint elevation and concavity of theST segment.

In patients with left ventricular hypertrophy,ST segment/T wave changes are encounteredin approximately 70% of cases, resulting fromaltered repolarisation of the ventricularmyocardium.10 These ST segment/T waveabnormalities are the new "norm" in patientswith electrocardiographic left ventricularhypertrophy and may mask and/or mimic theearly findings consistent with acute coronaryischaemia.11 Left ventricular hypertrophy isassociated with poor R wave progression andloss of the septal R wave in the right tomid-precordial leads, most commonly produc-ing a QS pattern. In general, these QScomplexes are located in leads Vi and V2,rarely extending beyond lead V3 (figs 1, 6, and7A, B). As predicted by the concept ofappropriate discordance (that is, the terminalportion of the QRS complex and STsegment/T wave are located on opposites sidesof the isoelectric baseline; fig 7C), ST segmentelevation is encountered in this distributionalong with prominent T waves. The STsegment elevation seen in this distribution maybe greater than 5 mm in height (figs 6 and 7A,B). The initial, up-sloping portion of the STsegment/T wave complex is frequently concavein left ventricular hypertrophy compared withthe either flattened or convex pattern observedin the AMI patient (fig 7C).1" This morpho-logical feature is imperfect; early AMI mayreveal such a concave feature. Another featureof left ventricular hypertrophy related STsegment/T wave change is its relative perma-nence; these changes are very unlikely tochange during the initial evaluation. This rela-tive difference in the longevity of the STsegmentVT wave changes in the two syndromeslends itself to differentiation using serialelectrocardiographic monitoring.

A B C

Figure 9 A comparison ofSTsegment elevation in (A) pericarditis, (B) BER, and (C)AMI. (A) Acute pericarditis is seen here with STE and PR segment depression. (B) BERwith ST segment elevation starting at the point. (C) AMI with convex ST segmentelevation. Note the concave nature of the ST segment elevation in acute pericarditis andBER compared with the convex elevation in AMI.

BENIGN EARLY REPOLARISATIONThe syndrome of BER, first described in 1936by Shipley and Hallaran, is felt to be a normalvariant, not indicative of underlying cardiacdisease.'2 BER has been reported to occur inapproximately 1% of the general population, inpersons of all age groups and varying racial andethnic backgrounds."3 In a large populationbased study, the mean age of patients withBER was 39 years with a range of 16-80 years.BER was seen predominantly in those patientsless than age 50 years and rarely encounteredin individuals over age 70 years (3.5%)." Menmanifest BER significantly more often thanwomen." For unknown reasons, BER is moreoften encountered in black men age 20-40years,'4 though some dispute this finding."3An ECG of BER (figs 2, 8, and 9B) includes

diffuse or widespread ST segment elevation(fig 2), upward concavity of the initial portionof the ST segment (figs 2, 8, and 9B), notchingor slurring of the terminal QRS complex (fig 2;lead V3) , and symmetric, concordant T wavesof large amplitude (figs 9, upper and middleexamples, and 9B)." The ST segment eleva-tion begins at the "J" (or junction point of theQRS complex and ST segment). The degree ofST segment elevation encountered in BER isusually less than 2 mm but may approach 5mm in certain individuals. Eighty to ninety percent of individuals show ST segment elevationless than 2 mm in the precordial leads and lessthan 0.5 mm in the limb leads; only 2% ofcases of BER manifest ST segment elevationgreater than 5 mm."3 16 The ST segment lookslike it has been lifted upwards evenly from theisoelectric baseline at the J point, preservingthe normal concavity of the initial, up-slopingportion of the ST segment/T wave complex(figs 2, 8, and 9B)." This ST segment elevationmorphology is a very important feature thatdistinguishes BER related ST segment eleva-tion from that associated with AMI. The Jpoint itself is frequently notched or irregular incontour and is considered highly suggestive-but not diagnostic-ofBER (fig 2; lead V3)."'3The degree of J point elevation is usually lessthan 3.5 mm." Prominent T waves of largeamplitude and slightly asymmetric morphol-ogy are also encountered; the T waves mayappear "peaked," suggestive of the hyperacuteT wave encountered in AMI. The prominent Twaves are concordant with the QRS complexand are usually found in the precordial leads.The height of the T waves in BER ranges fromapproximately 6.5 mm in the precordial distri-bution to 5 mm in the limb leads."'5The degree of ST segment elevation in BER

is usually greatest in the mid to left precordialleads (leads V2 -V5), and less often found inthe limb leads. One large series reported thatthe limb leads show ST segment elevation inonly 45% of cases of BER. "Isolated" BER inthe limb leads (no ST segment elevation in theprecordial leads) is a very rare finding." 16 Such"isolated" ST segment elevation in the inferior(II, III, and aVF) or lateral (I and aVL) leadsshould prompt consideration of another expla-nation for STE.

on Septem

ber 18, 2020 by guest. Protected by copyright.

http://emj.bm

j.com/

J Accid E

merg M

ed: first published as 10.1136/emj.16.6.433 on 1 N

ovember 1999. D

ownloaded from

Brady, Morris

LEFT VENTRICULAR ANEURYSMLeft ventricular aneurysm (LVA), also de-scribed as dyskinetic ventricular segment, isdefined as a localised area of infarcted myocar-dium which bulges outward during bothsystole and diastole. LVAs most often are notedafter large anterior wall events but may also beencountered after inferior and posterior wallAMIs. In most cases, the LVA is manifestedelectrocardiographically by varying degrees ofST segment elevation, which may be difficultto distinguish from ST segment changes due toAMI-particularly in the patient with chestpain with known past AMI." The actual STsegment elevation itself is felt to result fromeither a current of injury originating fromviable yet ischaemic myocytes in the aneurysmor from mechanical wall stress caused by trac-tion on the normal, adjacent myocardium.LVA is characterised electrocardiographi-

cally by persistent ST segment elevation seenseveral weeks after AMI. Because of thefrequent anterior location of LVA, ST segmentelevation is most often observed leads I, aVL,and V1-V6. Of course, the inferior wall LVAwould be manifested on the surface ECG byST segment elevation in the inferior leads asseen in case 3 (fig 3); such ST segmentelevation, however, is usually less pronouncedthan the ST segment changes seen in the ante-rior leads. The actual ST segment abnormalitydue to the LVA may present with varying mor-phologies, ranging from obvious, convex STsegment elevation (fig 3) to minimal, concaveelevations (fig 10). The distinction from STsegment elevation in the AMI patient may bedifficult." Reciprocal change, which is a notinfrequent electrocardiographic feature ofAMI, strongly suggests that the current STsegment changes results at least in part fromacute infarction. Patients with LVA, usually theresult of extensive anterior wall infarction, willfrequently also have significant Q waves in thesame distribution. The simultaneous appear-ance of the Q wave is not a feature thatunquestionably supports the electrocardio-graphic diagnosis of LVA; the doctor mustrecall that Q waves may appear as early as twohours after the onset of transmural AMI. Thedynamic nature of AMI related ST segmentelevation compared with the often static ST

V /1IFigure 11 Acute pericarditis with ST segment elevation in all three examples (upper leadIII (left), middle lead V2 (middle), and lower lead V4 (right)) as well as PR segmentdepression in the upper (left) and lower (right) examples. Once again, note the concavemorphology of the ST segment elevation, suggesting a non-infarction cause of the STsegment change. The shaded areas refer to the concave portion of the ST segment; thearrows indicate the PR segment depression.

segment character in LVA makes both acomparison with past ECGs as well as the useof serial ECGs of considerable diagnosticvalue.

ACUTE PERICARDITISAcute pericarditis, a diffuse inflammation ofthe pericardial sac and superficial myocar-dium, has a number of underlying causesincluding infections, immunological disorders,uraemia, trauma, malignancy, cardiac ischae-mia, AMI, as well as a multitude of other aeti-ologies. The clinical presentation of acute peri-carditis can be confused with acute coronaryischaemia. The difficulty in distinguishingacute myopericarditis from AMI, coupled withan increasing emphasis on rapid revascularisa-tion treatments in patients with acute infarc-tion, has led to inadvertent administration ofthrombolytic agents to patients with acutepericarditis.7 18

It has been reported that up to 90% ofpatients with acute myopericarditis have ab-normalities on the ECG.'9 Classically, severalstages of electrocardiographic change havebeen described involving ST segment eleva-tion, PR segment depression, T wave inver-sion, and normalisation." In general, stages1-3 are seen over hours to days but stage 4 maynot be reached for several weeks. Further,patients may not manifest all characteristicelectrocardiographic features of pericarditis-that is, the chest pain patient may present withstage 1 findings with progression directly tostage 4. Fewer than half of the patients withacute myopericarditis, however, evolve throughall stages.20ST segment elevation seen in patients with

stage 1 pericarditis is usually less than 5 mm inheight, observed in numerous leads, and char-acterised by a concavity to its initial up-slopingportion (fig 4). In some instances, the ST seg-ment elevation may actually be obliquely flat(inferior leads of fig 4). The ST segment eleva-tion caused by acute pericarditis is usuallynoted in all leads except VI (fig 4); reciprocalST segment depression is also seen in lead aVR(fig 4) and occasionally in lead V1. The STsegment elevation is most often seen in manyleads simultaneously, though it may be limitedto a specific anatomic segment. If the process isfocal, the inferior wall is often involved withleads II, II, and aVF commonly affected.PR segment depression associated with peri-

carditis perhaps is the most helpful feature inarriving at the correct electrocardiographicdiagnosis; such a finding has been described as"almost diagnostic" for acute pericarditis (figs4 and 1 1; upper and lower examples)." Recip-rocal PR segment elevation is seen in leadaVR-and may be easier to view in certaincases (fig 10).

OTHER SYNDROMESNumerous other clinical syndromes maypresent with electrocardiographic ST segmentelevation, including the various ventricularpaced rhythms, cardiomyopathies, acute myo-carditis, hypothermia, hyperkalaemia, pre-excitation syndromes, and acute abdominal

Figure 10 Left ventricularaneurysm in lead V2 withconcave ST segmentelevation.

WI.d../.

438

on Septem

ber 18, 2020 by guest. Protected by copyright.

http://emj.bm

j.com/

J Accid E

merg M

ed: first published as 10.1136/emj.16.6.433 on 1 N

ovember 1999. D

ownloaded from

ST segment elevation syndromes 439

and central nervous system disorders. Thesesyndromes will be discussed in future reports;left bundle branch block has been discussed inan earlier report.Conflict of interest: none.Funding: none.

1 Muller DW, Topol EJ. Selection of patients with acute myo-cardial infarction for thrombolytic therapy. Ann Intern Med1990;113:949-60.

2 Kleiman NS, White HD, Ohman EM, et al. Mortality within24 hours of thrombolysis for myocardial infarction: theimportance of early reperfusion. Circulation 1994;90:2658-65.

3 Lee TH, Weisberg MC, Brand DA, et al. Candidates forthrombolysis among emergency room patients with acutechest pain: potential true and false-positive rates. AnnIntern Med 1989;110:957-62.

4 GUSTO Investigators. An international randomized trialcomparing four thrombolytic strategies for acute myocar-dial infarction. NEnglJMed 1993;329:673-82.

5 Rude RE, Poole WK, Muller JE, et al. Electrocardiographicand clinical criteria for recognition of acute myocardial inf-arction based on analysis of 3,697 patients. Am J7 Cardiol1983;52:936-42.

6 Otto LA, Aufderheide TP. Evaluation of ST segment eleva-tion criteria for the prehospital electrocardiographicdiagnosis of acute myocardial infarction. Ann Emerg Med1994;23: 17-24.

7 Miller DH, Kligfield P, Schreiber TL, et al. Relationship ofprior myocardial infarction to false-positive electrocardio-graphic diagnosis of acute injury in patents with chest pain.Arch Intern Med 1987;147:257-61.

8 Sharkey SW, Berger CR, Brunette DD, et al. Impact of theelectrocardiogram on the delivery of thrombolytic therapyfor acute myocardial infarction. AmJ Cardiol 1994;73:550-3.

9 Larsen GC, Griffith JL, Beshansky JR, et al. Electrocardio-graphic left ventricular hypertrophy in patients withsuspected acute cardiac ischemia-its influence on diagno-sis, treatment, and short-term prognosis. Jf Gen Intern Med1994;9:666-73.

10 Huwez FU, Pringle SD, Macfarlane FW. Variable patternsof ST-T abnormalities in patients with left ventricularhypertrophy and normal coronary arteries. Br Heart J1992;67:304-7.

11 Aufderheide TP, Brady WJ. Electrocardiography in thepatient with myocardial ischemia or infarction. In: GiblerWB, Aufderheide TP, eds. Emergency cardiac care. 1st Ed.St Louis: Mosby, 1994: 169-216.

12 Shipley RA, Hallaran WR. The four-lead electrocardiogramin two hundred normal men and women. Am HeartJ 1936;11:325-45.

13 Mehta MC, Jain AC. Early repolarization on scalar electro-cardiogram. Am J Med Sci 1995;309:305-1 1.

14 Thomas J, Harris E, Lassiter G. Observations on the T waveand S-T segment changes in the precordial electrocardio-gram of 320 young negro adults. Am Jf Cardiol 1960;5:468-74.

15 Wasserburger RM, Alt WJ, Lloyd C. The normal RS-T seg-ment elevation variant. Am J Cardiol 1961;8:184-92.

16 Kabara H, Phillips J. Long-term evaluation of early repolari-zation syndrome (normal variant RS-T segment elevation).AmJ7 Cardiol 1976;38:157-61.

17 Millaire A, De Groote P, Decoulx E, et al. Outcome afterthrombolytic therapy of nine cases of pericarditis misdiag-nosed as myocardial infarction. Eur Heart J 1995;16:333-6.

18 Khoury NE, Borzak S, Gokli A, et al. Inadvertent thrombo-lytic administration in patients without myocardialinfarction: clinical features and outcome. Ann Emerg Med1996;28:289-96.

19 Shabetai R. Acute myppericarditis. Cardiol Clin 1990;8:639-81.

20 Marinella MA. Electrocardiographic manifestations anddifferential diagnosis of acute myopericarditis. Am FamPhysician 1990;57:699-705.

on Septem

ber 18, 2020 by guest. Protected by copyright.

http://emj.bm

j.com/

J Accid E

merg M

ed: first published as 10.1136/emj.16.6.433 on 1 N

ovember 1999. D

ownloaded from